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  • Indomethacin Reduces Lipid Peroxidation in Rat Brain Homogenate by Binding Fe2+

    Author(s)
    Anoopkumar-Dukie, S
    Lack, B
    McPhail, K
    Nyokong, T
    Lambat, Z
    Maharaj, D
    Daya, S
    Griffith University Author(s)
    Anoopkumar-Dukie, Shailendra
    Year published
    2003
    Metadata
    Show full item record
    Abstract
    One of the hallmarks of Alzheimer's disease (AD) is the progressive degeneration of cholinergic neurons in the cerebral cortex and hippocampus. It is generally accepted that this neuronal degeneration is due to free-radical-induced damage. These free radicals attack vital structural components of the neurons. This implies that agents that reduce free radical generation could potentially delay the progression of AD. Free radical generation in the brain is assisted by the presence of iron, required by the Fenton reaction. Thus, agents that reduce iron availability for this reaction could potentially reduce free radical formation. ...
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    One of the hallmarks of Alzheimer's disease (AD) is the progressive degeneration of cholinergic neurons in the cerebral cortex and hippocampus. It is generally accepted that this neuronal degeneration is due to free-radical-induced damage. These free radicals attack vital structural components of the neurons. This implies that agents that reduce free radical generation could potentially delay the progression of AD. Free radical generation in the brain is assisted by the presence of iron, required by the Fenton reaction. Thus, agents that reduce iron availability for this reaction could potentially reduce free radical formation. Since non steroidal anti-inflammatory drugs (NSAIDS) have been shown to reduce the severity of AD, we investigated the possible mechanism by which indomethacin could afford neuroprotection. Our results show that indomethacin (1 mM) is able to reduce the iron-induced rise in lipid peroxidation in rat brain homogenates. In addition, our NMR data indicate that indomethacin binds the Fe2+/Fe3+ ion. This was confirmed by a study using UV/Vis spectrophotometry. The results imply that indomethacin provides a neuroprotective effect by binding to iron and thus making it unavailable for free radical production.
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    Journal Title
    Metabolic Brain Disease
    Volume
    18
    Issue
    1
    DOI
    https://doi.org/10.1023/A:1021958016928
    Subject
    Clinical sciences
    Clinical sciences not elsewhere classified
    Neurosciences
    Publication URI
    http://hdl.handle.net/10072/32989
    Collection
    • Journal articles

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